ANTI

ANTI-INFLAMMATORY AGENTS FOR

SCHIZOPHRENIA

Norbert Müller, Michael Riedel, M.

Ackenheil, Markus J. Schwarz

Psychiatric and Psychotherapeutic

Hospital, Ludwig-Maximilians-University, Nußbaumstr. 7, 80336, Müchen

Alterations of the immune system in

schizophrenia have been described over the last century.  Several lines of

evidence suggest that an inflammatory process in the central nervous system

(CNS) may play a role in schizophrenia.  Although there is a controverse

discussion of the role of immunological findings in schizophrenia and more

insight into the pathological process is needed, we performed a systematic

clinical trial of anti-inflammatory treatment in schizophrenia using the

selective cycloxgenase-2 inhibitor celecoxib in order to evaluate the

therapeutic effects.   This study was performed as a single-center

double-blind, placebo-controlled randomized, add-on, parallel-group evaluation

of risperidone and celecoxib versus risperidone and placebo.  Fifty

schizophrenic patients were included in the study, of whom 25 received 2-6 mg

risperidone/day and placebo, and 25 risperidone and 400 mg/day celecoxib for 5

weeks after wash-out.  Both groups of schizophrenic patients showed

significant improvement on the overall positive- and negative syndrome scale

(PANSS), and on all subscales, during the five week treatment with

risperidone.  However, the celecoxib add-on therapy group had significantly

more decrease in the PANSS total score over weeks 2-4 (ANCOVA).  The

results show that additional treatment with celecoxib has significant positive

effects on the schizophrenic total psychopathology.  Moreover, since

treatment with an immunomodulatory drug shows beneficial effects on the

schizophrenic symptomatology, this result represents another indication that

immune dysfunction in schizophrenia is not just an epiphenomen but related to

the pathomechanism of the disorder.  In parallel immune parameters were

estimated and the immunological results will be discussed regarding an

immunological model of schizophrenia.

This work was supported by the Vada and

Theodore Stanley Foundation.